Circadian rhythms and sleep in children with autism

Glickman, Gena

doi:10.1016/j.neubiorev.2009.11.017

Cited by 150 publications

(119 citation statements)

References 156 publications

(268 reference statements)

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“…This theory is supported by evidence that children with autism exhibit abnormal cortisol and melatonin profiles (see Glickman 2010, for a review). The role of melatonin as a mechanism through which sleep disturbances manifest in children with ASD is also exemplified by the finding that such sleep disturbances are attenuated by pharmacological administration of melatonin (Paavonen et al 2003).…”

Section: Restless Legs Syndrome (Rls): Rls Is Characterised By Unpleamentioning

confidence: 89%

Sleep in Childhood and Adolescence: Age-Specific Sleep Characteristics, Common Sleep Disturbances and Associated Difficulties

Barclay¹,

Gregory²

2013

The Neurobiology of Childhood

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Sleep changes throughout the lifespan, with particularly salient alterations occurring during the first few years of life, as well as during the transition from childhood to adolescence. Such changes are partly the result of brain maturation; complex changes in the organisation of the circadian system; as well as changes in daily routine, environmental demands and responsibilities.Despite the automaticity of sleep, given that it is governed by a host of complex mechanisms, there are times when sleep becomes disturbed. Sleep disturbances in childhood are common and may stem from behavioural difficulties or abnormalities in physiological processes and, in some cases manifest into diagnosable sleep disorders. As well as occurring exclusively, childhood sleep disturbances often co--occur with other difficulties. The purpose of this chapter is to outline the neurobiology of typical sleep/wake processes, and describe changes in sleep physiology and architecture from birth to adulthood. Furthermore, common childhood sleep disorders are described as are their associations with other traits, including all of the syndromes presented in this handbook: ASDs, ADHD, schizophrenia, and emotional/ behavioural difficulties. Throughout, we attempt to explain possible mechanisms underlying these disorders and their associations.

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Section: Restless Legs Syndrome (Rls): Rls Is Characterised By Unpleamentioning

confidence: 89%

Sleep in Childhood and Adolescence: Age-Specific Sleep Characteristics, Common Sleep Disturbances and Associated Difficulties

Barclay¹,

Gregory²

2013

The Neurobiology of Childhood

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“…28 Defects in circadian rhythm may also affect the daily timing of neurobehavioral and endocrine functions. 29 Circadian rhythm defects seen in ASD are thought to contribute not only to the sleep disturbances but also to behavior, learning, and other phenotypes seen in these patients. 29 2q23.1 deletion syndrome, MBD5, and sleep In this study, we show that individuals with del 2q23.1 syndrome have sleep disturbances.…”

Section: Discussionmentioning

confidence: 99%

“…29 Circadian rhythm defects seen in ASD are thought to contribute not only to the sleep disturbances but also to behavior, learning, and other phenotypes seen in these patients. 29 2q23.1 deletion syndrome, MBD5, and sleep In this study, we show that individuals with del 2q23.1 syndrome have sleep disturbances. These sleep studies further support previous reports regarding del 2q23.1 patients' sleep habits.…”

Section: Discussionmentioning

confidence: 99%

MBD5 haploinsufficiency is associated with sleep disturbance and disrupts circadian pathways common to Smith–Magenis and fragile X syndromes

et al. 2014

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Individuals with autism spectrum disorders (ASD) who have an identifiable single-gene neurodevelopmental disorder (NDD), such as fragile X syndrome (FXS, FMR1), Smith-Magenis syndrome (SMS, RAI1), or 2q23.1 deletion syndrome (del 2q23.1, MBD5) share phenotypic features, including a high prevalence of sleep disturbance. We describe the circadian deficits in del 2q23.1 through caregiver surveys in which we identify several frequent sleep anomalies, including night/early awakenings, coughing/ snoring loudly, and difficulty falling asleep. We couple these findings with studies on the molecular analysis of the circadian deficits associated with haploinsufficiency of MBD5 in which circadian gene mRNA levels of NR1D2, PER1, PER2, and PER3 were altered in del 2q23.1 lymphoblastoid cell lines (LCLs), signifying that haploinsufficiency of MBD5 can result in dysregulation of circadian rhythm gene expression. These findings were further supported by expression microarrays of MBD5 siRNA knockdown cells that showed significantly altered expression of additional circadian rhythm signaling pathway genes. Based on the common sleep phenotypes observed in del 2q23.1, SMS, and FXS patients, we explored the possibility that MBD5, RAI1, and FMR1 function in overlapping circadian rhythm pathways. Bioinformatic analysis identified conserved putative E boxes in MBD5 and RAI1, and expression levels of NR1D2 and CRY2 were significantly reduced in patient LCLs. Circadian and mTOR signaling pathways, both associated with sleep disturbance, were altered in both MBD5 and RAI1 knockdown microarray data, overlapping with findings associated with FMR1. These data support phenotypic and molecular overlaps across these syndromes that may be exploited to provide therapeutic intervention for multiple disorders. Significant sleep problems are highly prevalent in individuals with ASD. 2 Parents of children with ASD report 50-80% prevalence of sleep problems compared with a 9-50% prevalence rate reported by parents of age-matched typically developing children. 2 Common sleep etiological factors that are present in children with ASD are rapid eye movement sleep abnormalities, dysregulation of melatonin synthesis, difficulty in settling to sleep, night waking, irregular sleep patterns, short-duration sleep, and daytime sleepiness. 2,3 Persistent sleep problems are thought to adversely affect cognitive, physical, and social function, learning, mood, and behavior in these individuals and, in addition, cause significant stress for families and caretakers. 3 Better understanding of the sleep difficulties experienced by children with ASD may reduce the adverse effects and decrease family stress, possibly with targeted therapies.

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“…Autism has been associated with atypical sleep patterns and circadian rhythms [135]. Polymorphisms in ASMT (involved in melatonin synthesis), paralleled by reduced levels of circulating melatonin, have been reported in autism [136].…”

Section: Suggested Roles Of the Ecb System In Autismmentioning

confidence: 99%

Endocannabinoid Signaling in Autism

et al. 2015

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Autism spectrum disorder (ASD) is a complex behavioral condition with onset during early childhood and a lifelong course in the vast majority of cases. To date, no behavioral, genetic, brain imaging, or electrophysiological test can specifically validate a clinical diagnosis of ASD. However, these medical procedures are often implemented in order to screen for syndromic forms of the disorder (i.e., autism comorbid with known medical conditions). In the last 25 years a good deal of information has been accumulated on the main components of the Bendocannabinoid (eCB) system^, a rather complex ensemble of lipid signals (Bendocannabinoids^), their target receptors, purported transporters, and metabolic enzymes. It has been clearly documented that eCB signaling plays a key role in many human health and disease conditions of the central nervous system, thus opening the avenue to the therapeutic exploitation of eCB-oriented drugs for the treatment of psychiatric, neurodegenerative, and neuroinflammatory disorders. Here we present a modern view of the eCB system, and alterations of its main components in human patients and animal models relevant to ASD. This review will thus provide a critical perspective necessary to explore the potential exploitation of distinct elements of eCB system as targets of innovative therapeutics against ASD.Key Words Autism spectrum disorder . endocannabinoid system . fragile X syndrome . metabolic regulation . reward system The Endocannabinoid SystemTwenty-five years after the cloning and expression of a complementary DNA that encoded a G protein-coupled receptor, named type-1 cannabinoid (CB 1 ) receptor [1], there is a good deal of information on the main components of the so-called Bendocannabinoid (eCB) system^, as well as on its role in controlling cannabinergic signaling in human health and disease [2][3][4]. Anandamide (AEA) and 2-arachidonoylglycerol (2-AG) are the most active eCBs as yet identified, although this family of bioactive lipids includes other arachidonic acid (AA) derivatives with cannabimimetic properties (i.e., noladin ether, virodhamine, N-arachidonoyldopamine, to name but a few). The classical dogma that eCBs are synthesized and released Bon demand^upon (patho)physiological stimuli has been recently revisited on the basis of unexpected evidence for intracellular reservoirs and transporters of eCBs. These new entities have been shown to drive intracellular trafficking of eCBs, adding a new dimension to the regulation of their biological activity [5]. To date, several metabolic routes have B. Chakrabarti, A. Persico and N. Battista are equal first authors.

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Circadian rhythms and sleep in children with autism

Cited by 150 publications

References 156 publications

Sleep in Childhood and Adolescence: Age-Specific Sleep Characteristics, Common Sleep Disturbances and Associated Difficulties

Sleep in Childhood and Adolescence: Age-Specific Sleep Characteristics, Common Sleep Disturbances and Associated Difficulties

MBD5 haploinsufficiency is associated with sleep disturbance and disrupts circadian pathways common to Smith–Magenis and fragile X syndromes

Endocannabinoid Signaling in Autism

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